Treatment of IgA nephropathy: an overview

Summary: Any form of therapy for IgA nephritis (IN) must be rational and practical. the least toxic agent should be chosen with a view to life‐long therapy for patients with poor prognostic indices. While we accept that there is no cure for the disease, we could still offer these patients therapeutic measures to retard the pro gression to end‐stage renal failure (ESRF). In IN there is a general defect in clearance of immune complexes. to limit the amount of mesangial deposits you can reduce antigen load, downregulate lymphokines and employ enzymes to remove glomerular deposits. the use of steroids in treatments have had varying results, some reporting reduction of proteinuria and stability of renal function. A short course of cyclosporine A can reduce proteinuria. Dual therapy with dipyridamole and low dose warfarin can retard progression to ESRF. Results of fish oil therapy are variable, except for two studies, most of the other studies have reported no bene ficial effects. Urokinase have been shown to decrease proteinuria and stabilize renal function. Angiotensin converting enzyme (ACE) inhibitors are proven to retard progression to ESRF by decreasing intraglomerular hypertension. Other therapeutic measures have included low protein and gluten‐free diet and, in some cases a tonsillectomy has blunted disease progression. the single most important factor in treatment is adequate control of systemic hypertension to retard progression of the disease. For patients with the nephrotic syndrome with selective proteinuria the response to prednisolone and cyclophosphamide is usually good. Future therapeutic strategies would include inhibition of mediators and cytokines (platelet‐derived growth factor [PDGF]) antagonist, tumour necrosis factor (TNF) inhibitor) and gene therapy.